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Biomedical subjects

R Rossi

Publications and source records attributed to R Rossi.

At least 55 records · Page 3Linked to original sources

Diagnostic of sexual perversions.

Sexual perversion is a very controversial matter and difficult to define because, instead of being analyzed as a clinical phenomenon, is seen as a social one: society establishes what is perverse and what is not. If we analyzed the evolution of sexuality we would find many sexual practices considered nowadays forbidden. For example, we consider perverse sexual acts replacing the coitus but we accept as normal what were previously considered deviant forms of sexual intercourse that simply accompany the coitus. In reality there is not a definite boundary between "normality" and "perversion" as each one of us shows a certain grade of perversion that can be disclosed sometimes in imperceptible or harmless ways. Contemporary sexology believes that the worst perversions do not have to implicate genitalia but can also consist of behaviors hiding their own sexual nature and acting as sexual surrogates, such as kleptomania and pyromania that only apparently seem to have nothing to do with sex.

Diagnosis, Differential↗

Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study.

BACKGROUND: To test the hypothesis of general atherosclerotic plaque destabilization during acute coronary syndrome (ACS), the present study sought to analyze the 3 coronary arteries by systematic intravascular ultrasound scan (IVUS). METHODS AND RESULTS: Seventy-two arteries were explored in 24 patients referred for percutaneous coronary intervention after a first ACS with troponin I elevation. Fifty plaque ruptures (mean, 2.08 per patient; range, 0 to 6) were diagnosed by the association of a ruptured capsule with intraplaque cavity. Plaque rupture on the culprit lesion was found in 9 patients (37.5%). At least 1 plaque rupture was found somewhere other than on the culprit lesion in 19 patients (79%). These lesions were in a different artery than the culprit artery in 70.8% and were in both other arteries in 12.5% of these 24 patients. Complete IVUS examination of all 3 coronary axes in patients who had experienced a first ACS revealed that multiple atherosclerotic plaque ruptures were detected by IVUS; these multiple ruptures were present simultaneously with the culprit lesion; they were frequent and located (in three quarters of cases) on the 3 principal coronary trunks; and the multiple plaque ruptures in locations other than on the culprit lesion were less severe, nonstenosing, and less calcified. CONCLUSION: Although one single lesion is clinically active at the time of ACS, the syndrome seems nevertheless associated with overall coronary instability.

Acute Disease↗

Methionine oxidation as a major cause of the functional impairment of oxidized actin.

A significant specific increase in the actin carbonyl content has been recently demonstrated in human brain regions severely affected by the Alzheimer's disease pathology, in postischemic isolated rat hearts, and in human intestinal cell monolayers following incubation with hypochlorous acid (HOCl). We have very recently shown that exposure of actin to HOCl results in the immediate loss of Cys-374 thiol, oxidation of some methionine residues, and, at higher molar ratios of oxidant to protein, increase in protein carbonyl groups, associated with filament disruption and inhibition of filament formation. In the present work, we have studied the effect of methionine oxidation induced by chloramine-T (CT), which at neutral or slightly alkaline pH oxidizes preferentially Met and Cys residues, on actin filament formation and stability utilizing actin blocked at Cys-374. Methionines at positions 44, 47, and 355, which are the most solvent-exposed methionyl residues in the actin molecule, were found to be the most susceptible to oxidation to the sulfoxide derivative. Met-176, Met-190, Met-227, and Met-269 are the other sites of the oxidative modification. The increase in fluorescence associated with the binding of 8-anilino-1-naphtalene sulfonic acid to hydrophobic regions of the protein reveals that actin surface hydrophobicity increases with oxidation, indicating changes in protein conformation. Structural alterations were confirmed by the decreased susceptibility to proteolysis and by urea denaturation curves. Oxidation of some critical methionines (those at positions 176, 190, and 269) causes a complete inhibition of actin polymerization and severely affects the stability of actin filaments, which rapidly depolymerize. The present results would indicate that the oxidation of some critical methionines disrupts specific noncovalent interactions that normally stabilize the structure of actin filaments. We suggest that the process involving formation of actin carbonyl derivatives would occur at an extent of oxidative insult higher than that causing the oxidation of some critical methionine residues. Therefore, methionine oxidation could be a damaging event preceding the appearance of carbonyl groups on actin and a major cause for the functional impairment of the carbonylated protein recently observed both in vivo and in vitro.

Actins↗

Randomized controlled trial of single-agent paclitaxel versus cyclophosphamide, doxorubicin, and cisplatin in patients with recurrent ovarian cancer who responded to first-line platinum-based regimens.

PURPOSE: To assess the activity, efficacy, and tolerability of single-agent paclitaxel and a platinum-containing regimen in previously treated patients with recurrent ovarian cancer. PATIENTS AND METHODS: Patients who achieved complete remission with platinum-based regimens and whose disease recurred after a progression-free interval of more than 12 months were included in the study. Every 21 days, patients received paclitaxel 175 mg/m(2) intravenously (IV) over 3 hours or cyclophosphamide 500 mg/m(2), doxorubicin 50 mg/m(2), and cisplatin 50 mg/m(2) (CAP) IV. RESULTS: Between June 1992 and May 1995, 97 consecutive patients with assessable or measurable disease were randomized to paclitaxel (n = 50) or CAP (n = 47). The median number of cycles on each arm was six. Toxicities included grade 3/4 leukopenia (4% for paclitaxel v 34% for CAP), grade 3/4 neutropenia (13% v 36%), grade 1/2 myalgia (19% v 4%), allergic reactions (15% v 2%), and grade 2/3 nausea and vomiting (17% v 51%). Complete responses were achieved in 17% and 30% of patients receiving paclitaxel and CAP, respectively, and partial responses were achieved in 28% and 25%, respectively (P =.062). At a median follow-up time of 49 months, median progression-free intervals were 9 months for paclitaxel and 15.7 months for CAP (Cox analysis: hazards ratio [HR], 0.60; 95% confidence interval [CI], 0.37 to 0.97; P =.038); median overall survival times were 25.8 months for paclitaxel and 34.7 months for CAP (Cox analysis: HR, 0.58; 95% CI, 0.34 to 0.98; P =.043). CONCLUSION: Rechallenge with either single-agent paclitaxel or platinum-based chemotherapy is effective in this patient population. Preliminary results suggest that single-agent paclitaxel may not be as active as platinum-based chemotherapy in recurrent ovarian cancer. Larger randomized trials are needed.

Adult↗

Cathamenial pneumothorax.

Cathamenial pneumothorax is a relatively low-frequency pathology (approximately 100 cases cited in the literature) characterized by recurrent pneumothorax episodes during the menstruation period. We report on a 34-year-old female patient who had recurrent pneumothorax that did not respond to chest drainage and whose presentation was directly related to the menstruation period. Our patient also had a significant clinical record for pelvic endometriosis. She underwent video-assisted thoracoscopic exploration (VATS) of the pleural cavity and dystrophic parenchymal blebs of the middle lobe were found. An atypical resection of the bollous tissue was performed and pleurodesis completed the intervention. During VATS no ectopic endometriosis foci or diaphragmatic fenestrations (widely considered as a possible cause of this clinical picture) were evidenced.

Adult↗

Protein thiols and glutathione influence the nitric oxide-dependent regulation of the red blood cell metabolism.

Nitric oxide (NO) can modulate red blood cell (RBC) glycolysis by translocation of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPD) (EC 1.2.1.12) from the cytosolic domain of the membrane protein band 3 (cdb3) in the cytosol. In this study we have investigated which NO-reactive thiols might be influencing GAPD translocation and the specific role of glutathione. Two highly reactive Cys residues were identified by transnitrosylation with nitrosoglutathione (GSNO) of cdb3 and GAPD (K(2) = 73.7 and 101.5 M(-1) s(-1), respectively). The Cys 149 located in the catalytic site of GAPD is exclusively involved in the GSNO-induced nitrosylation. Reassociation experiments carried out at equilibrium with preparations of RBC membranes and GAPD revealed that different NO donors may form -SNO on, and decrease the affinity between, GAPD and cdb3. In intact RBC, the NO donors 3-morpholinosydnonimine (SIN-1) and peroxynitrite (ONOO(-)) significantly increased GAPD activity in the cytosol, glycolysis measured as lactate production, and energy charge levels. Our data suggest that ONOO(-) is the main NO derivative able to cross the RBC membrane, leading to GAPD translocation and -SNO formation. In cell-free experiments and intact RBC, diamide (a thiol oxidant able to inhibit GAPD activity) was observed to reverse the effect of SIN-1 on GAPD translocation. The results demonstrate that cdb3 and GAPD contain reactive thiols that can be transnitrosylated mainly by means of GSNO; these can ultimately influence GAPD translocation/activity and the glycolytic flux.

Anion Exchange Protein 1, Erythrocyte↗

In vitro study of methylmercury in blood of bottlenose dolphins (Tursiops truncatus).

The biochemical behavior of methylmercury (MeHg) in dolphin blood was investigated in vitro. MeHg distribution between plasma and erythrocytes and its release from erythrocytes into plasma or medium without SH group was determined. At the subcellular level its distribution among different thiol-containing molecules was also investigated in erythrocytes and plasma. When blood was treated with 0.1 mM MeHg, about 98.1% was found in red cells and 1.9% in plasma; only 0.6% of MeHg present in the cellular compartment was bound to membranes. Hemoglobin (Hb) and albumin, principal proteins containing SH groups (PSH), and glutathione (GSH) appeared to be the main targets of MeHg in dolphin blood. Gel filtration of stroma-free hemolysate of treated red blood cells (RBCs) revealed that MeHg was almost equally present in high (52.5%) and low (47.5%) molecular weight fractions, whereas in plasma it only eluted with proteins (high molecular weight fractions). Hemoglobin was identified as the main intracellular protein binding MeHg. The exchange reaction of MeHg between GSH and dolphin hemoglobin was also evaluated and the equilibrium constants calculated.

Animals↗

Giant exophytic basal cell carcinoma treated with radiotherapy.

Basal cell carcinomas may attain giant proportions due primarily to recurrence or because the tumour is neglected. We report the case of a 66-year-old man who presented with a bleeding, polypoid, cutaneous tumour located on the left shoulder region of 13 years duration. The man had not received any previous treatment. The lesion was biopsied and histopathologically diagnosed as a solid type basal cell carcinoma with focal areas of squamous differentiation and keratinization. The man refused complete surgical removal and therefore was treated with roentgentherapy, with satisfactory results and no complications in the irradiated area. No recurrences had manifested after 1 year follow-up.

Aged↗

Autosomal recessive type of Adams-Oliver syndrome: prenatal diagnosis.

We report on three pregnancies complicated by Adams-Oliver syndrome in a consanguineous Turkish couple. Two cases were correctly diagnosed prenatally at 22+3 and 13+0 weeks gestation following the first case of Adams-Oliver syndrome in which severe anomalies of the extremities were observed at 26+5 weeks' gestation. In this first case, the diagnosis of Adams-Oliver syndrome was made following termination of pregnancy at 27+2 weeks' gestation. In all three cases, autopsy was performed. All fetuses showed anomalies of the extremities, aplasia cutis and symmetric defects of the skull, with bone being replaced by collagenous tissue. Although there have been numerous cases of the postnatal diagnosis of Adams-Oliver syndrome following termination of pregnancy, this is the first description of the prenatal diagnosis of this disorder.

Abortion, Induced↗

Increased intima-media thickness of the carotid artery wall, normal blood pressure profile and normal left ventricular mass in subjects with primary hyperparathyroidism.

OBJECTIVE: Despite the increasing evidence that primary hyperparathyroidism (PHPT) contributes to greater risk of cardiovascular morbidity and mortality, its exact role in the development of cardiovascular changes and its clinical significance are still controversial. Given the multiple influence of PHPT on the cardiovascular system, this study aimed to assess the effects of PHPT on blood pressure profile, and on features of the heart and arterial vessels in normotensive symptomless patients. DESIGN: Twenty patients (8 males and 12 females) with a median age of 51.5 years (range 44 to 65 years) were evaluated and the results were compared with those of 20 controls matched for age, gender and body mass index. Patients' parathyroid hormone levels ranged from 172 to 454 pg/ml and Ca levels ranged from 11.4 to 13.5 mg/dl. Fasting levels of glucose, insulin, total and high density lipoprotein cholesterol and triglycerides were within the normal range in all subjects recruited. METHODS: Twenty-four-hour blood pressure profile, left ventricle (LV) dimension and carotid artery anatomy were investigated, the latter two by ultrasonography. RESULTS: No difference was found between the patients and controls in blood pressure profile, when the following parameters were considered: supine systolic/diastolic pressure, average 24-h systolic, diastolic and mean arterial pressure, day-time mean arterial pressure and fall in nocturnal blood pressure (-17% and -18% respectively). Heart rate and all parameters of LV mass were similar in patients and controls. The only alteration found in patients was in significantly greater carotid intimal-medial thickness (IMT) (P<0.001). Atherosclerotic plaques were more frequent in patients than in controls, with a difference reaching a trend (40% vs 10%, chi(2)=4.8; P=0.091). Considering that the carotid IMT is considered to be a marker of systemic atherosclerosis, our finding suggests early atherosclerotic changes in PHPT. No correlation was found between the severity and cardiovascular manifestation of PHPT. CONCLUSIONS: Vascular changes may occur due to a combination of structural and functional impairments in PHPT patients, likely as a result of altered calcium metabolism and impaired equilibrium of other factors regulating vascular function. Both extent and duration of PHPT can play a relative role in the development of cardiovascular complications. Considering that PHPT is now recognized as a quite common and often symptomless endocrine disorder, the evidence of cardiovascular manifestation in normotensive patients, found by this morphological study, suggests a possible implication for the management of such patients. In this light, screening for abnormalities in cardiovascular system function should be recommended in all PHPT subjects.

Adult↗

The use of the small caliber JJ stent with anti-reflux valve in double kidney transplant. Personal experience.

BACKGROUND: In the experience of other authors, double kidney transplant have a higher complication rate (30%) if compared with single renal graft. In personal experience the use of small calibre ureteral stents with antireflux valve can reduce this complication rate. METHODS: From November 1999 to April 2001, at the A.S.O. S. Giovanni Battista in Turin, we performed 29 double kidney transplantations with the application of small calibre stents in 20 male and 9 female patients, aged 50-74 years. The uretero-neocystostomies were carried out according to Lich-Gregoire technique, and the JJ stents used were pediatric ones, 12 cm long and 4.8 Ch, with antireflux valve. RESULTS: We complained only 2 urological complications out of 58 anastomoses (distal unilateral ureteral necrosis in 1 case and total ureteral necrosis in the other). CONCLUSIONS: Complication rate is lower than in the literature: the authors suggest that the use of small calibre JJ stents can keep the complication rate low in double kidney transplant.

Aged↗

[Multiple ruptures of atherosclerotic plaques in acute coronary syndrome. Endocoronary ultrasonography study of three arteries].

The aim of this study was to assess the three coronary arteries systematically by endocoronary ultrasonography in patients with unstable angina to check the hypothesis of global destabilisation of atherosclerotic plaques in acute coronary syndromes (ACS). Sixty two coronary arteries were examined (2.6 per patient). Fifty plaque ruptures were diagnosed (2.08 per patient). Rupture of a plaque of the culprit lesion of the ACS was clearly detected in 9 patients (37.5%). At least one ruptured plaque on a site other than the culprit lesion was observed in 19 patients (79%), on another artery in 70.8% of cases and on two other arteries in 12.5% of cases. A complete endocoronary ultrasonic examination of the three coronary arteries in patients with a first ACS demonstrated that: multiple atherosclerotic plaque rupture may be detected by endocoronary ultrasonography; these multiple plaque ruptures occur simultaneously with the culprit lesion; they are frequent and can be situated on the three main coronary vessels and multiple plaque rupture other than the culprit lesion are less severe, non stenotic and less calcified. Thus, although a single lesion is clinically symptomatic, ACS seems to be associated with global coronary instability.

Acute Disease↗

The actin cytoskeleton response to oxidants: from small heat shock protein phosphorylation to changes in the redox state of actin itself.

Actin is the major constituent of the cytoskeleton of almost all the eukaryotic cells. In vitro experiments have indicated that oxidant-stressed nonmuscle mammalian cells undergo remarkable changes in their morphology and in the structure of the actin cytoskeleton, often resulting in plasma membrane blebbing. Although the microfilament network is one of the earliest targets of oxidative stress, the mechanism by which oxidants change both the structure and the spatial organization of actin filaments is still a matter of debate and far from being fully elucidated. Starting from the 2-fold role of oxidants as injurious by-products of cellular metabolism and essential participants in cell signaling and regulation, this review attempts to gather the most relevant information related to (i) the activation of mitogen-activated protein (MAP) kinase stress-activated protein kinase-2/p38 (SAPK2/p38) which, via MAP kinase-activated protein (MAPKAP) kinase 2/3, leads to the phosphorylation of the actin polymerization (F-actin) modulator 25/27 kDa heat shock protein (HSP25/27), whose phosphorylation is causally related to the regulation of microfilament dynamics following oxidative stress; (ii) the alteration of the redox state of actin or some actin regulatory proteins. The actin cytoskeleton response to oxidants is discussed on the basis of the growing body of evidence indicating the actin system as the most sensitive constituent of the cytoskeleton to the oxidant attack.

Actins↗

Ca2+ release induced by cyclic ADP ribose in mice lacking type 3 ryanodine receptor.

The action of cyclic-ADP-ribose was studied on calcium release from sarcoplasmic reticulum of skeletal muscles of neonatal and adult wild-type and RyR3-deficient mice. cADPR increased calcium efflux from microsomes, enhanced caffeine-induced calcium release, and, in 20% of the tests, triggered calcium release in single muscle fibers. These responses occurred only in the diaphragm of adult RyR3-deficient mice. cADPR action was abolished by ryanodine, ruthenium red, and 8-brome-cADPR. These results strongly favor a specific action of cADPR on RyR1. The responsiveness of RyR1 appears in adult muscles when RyR3 is lacking.

Adenosine Diphosphate Ribose↗

Actin carbonylation: from a simple marker of protein oxidation to relevant signs of severe functional impairment.

The number of protein-bound carbonyl groups is an established marker of protein oxidation. Recent evidence indicates a significant increase in actin carbonyl content in both Alzheimer's disease brains and ischemic hearts. The enhancement of actin carbonylation, causing the disruption of the actin cytoskeleton and the loss of the barrier function, has also been found in human colonic cells after exposure to hypochlorous acid (HOCl). Here, the effects of oxidation induced by HOCl on purified actin are presented. Results show that HOCl causes a rapidly increasing yield of carbonyl groups. However, when carbonylation becomes evident, some Cys and Met residues have been already oxidized. Covalent intermolecular cross-linking as well as some noncovalent aggregation of carbonylated actin have been found. The covalent cross-linking, unaffected by reducing and denaturing agents, parallels an increase in dityrosine fluorescence. Moreover, HOCl-mediated oxidation induces the progressive disruption of actin filaments and the inhibition of F-actin formation. The molar ratios of HOCl to actin that lead to inhibition of actin polymerization seem to have effect only on cysteines and methionines. The process that involves oxidation of amino acid side chains with formation of a carbonyl group would occur at an extent of oxidative insult higher than that causing the oxidation of some critical amino acid residues. Therefore, the increase in actin content of carbonyl groups found in vivo would indicate drastic oxidative modification leading to drastic functional impairments.

Actin Cytoskeleton↗